Dendritic cells (DC) are the most potent known antigenpresenting cells and are primarily responsible for sensitizing naıve T cells to antigen. DC activate T cells by supplying antigenic (signal 1) and co-stimulatory (signal 2) signals as well as an additional set of ‘‘third signals’’ that can profoundly affect T cell function [1].

For example, if the cytokine interleukin-12 (IL-12) is present during Th sensitization it is likely that Th1 polarization will occur, resulting in T cells that produce high levels of IFN-c and correspondingly less (or no) IL-4 and IL-5 [2]. Such cells can be highly effective for dealing with some intracellular parasites [3].On the other hand, the cytokines IL-23, IL-6, TGF-b and IL-1b have each been implicated by various groups [4–9] in promoting the development of IL-17-producing Th17 cells.

These Th17 cells appear highly effective against extracellular bacteria, particularly those that colonize mucosal surfaces [10], and have also been implicated in chronic inflammatory pathology associated with some autoimmune diseases [11,12]. Additional cytokines contribute to the development of other key Th phenotypes including Th2 and Treg [12,13]. It has therefore become increasingly clear that these individual Th phenotypes represent adaptations for dealing with particular types of infection, or otherwise regulating immune responses. In contrast, dysregulation of these differentiation programs could result in ineffective immune responses against pathogens, debilitating autoimmune pathologies, or perhaps even promotion of carcinogenesis [14].